Clinical, respiratory, haemodynamic, and metabolic determinants of lactate in heart failure

Abstract

Background: Lactate is an end-product of anaerobic cell metabolism. Although it is believed to have prognostic significance in heart failure (HF), data on the pathomechanisms that lead to lactate accumulation are scarce.

Aims: We aimed to determine the clinical, respiratory, biochemical, and haemodynamic correlates of lactate in HF.

Methods: Patients diagnosed with HF hospitalised in a single cardiac centre, who underwent haemodynamic monitoring, were included in this retrospective analysis.

Results: The population consisted of 93 patients (44 acute HF [AHF] and 49 chronic HF [CHF] cases). The mean age, left ventricular ejection fraction, and lactate level were 60 ± 13 years, 33% ± 17%, 1.4 ± 0.9 mmol/L, respectively. The mean cardiac index (CI), right atrial pressure (RAP) and pulmonary capillary wedge pressure (PCWP) were 2.2 ± 0.5 L/min/m², 8.7 ± 6 mmHg, and 18 ± 6 mmHg, respectively. AHF patients had significantly higher RAP, heart rate (HR), and levels of N-terminal pro–B-type natriuretic peptide and creatinine, compared to the CHF group. Both HR and natriuretic peptide level were correlated with lactate. Among haemodynamic indices, lactate correlated with CI (r = –0.25, p = 0.01). We found no correlation between lactate and RAP (p > 0.05) or PCWP (p > 0.05). There was no relationship between lactate and peripheral blood gases. Lactate was strongly correlated with mixed venous oxygen saturation (svO2) (r = –0.61, p < 0.05). HR, svO2, and systemic vascular resistance (SVR) were found to be independent determinants of lactate.

Conclusions: Lactate accumulation in HF is not a result of respiratory disturbances or hypoxaemia. Among haemodynamic indices, CI is correlated with lactate. The strongest determinants of lactate included svO2, SVR, and HR.